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首页> 外文期刊>Infection and immunity >NK Cells in Gamma-Interferon-Deficient Mice Suppress Lung Innate Immunity against Mycoplasma spp.
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NK Cells in Gamma-Interferon-Deficient Mice Suppress Lung Innate Immunity against Mycoplasma spp.

机译：γ-干扰素缺乏小鼠中的NK细胞抑制针对支原体属的肺固有免疫力。

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The purpose of this study was to examine the 100-fold difference in mycoplasma levels in lungs of gamma interferon knockout (IFN-γ?/?) mice compared to those seen with wild-type BALB/c mice at 3 days postinfection. NK cells secreted IFN-γ; however, their cytotoxic granule extracts failed to kill mycoplasma. We found a conundrum: the clearance of organisms was as effective in NK-depleted IFN-γ?/? animals as in wild-type mice (with both IFN-γ and NK cells). NK+ IFN-γ?/? animals had high mycoplasma burdens, but, after NK-like cell depletion, mycoplasma numbers were controlled. Essentially, IFN-γ was important in animals with NK-like cells and unimportant in animals without NK cells, suggesting that IFN-γ counters deleterious effects of NK-like cells. Impairment of innate immunity in IFN-γ?/? mice was not due to NK-like cell killing of macrophages. The increased levels of inflammatory cytokines and neutrophils in lung fluids of NK+ IFN-γ?/? mice were reduced after NK cell depletion. In summary, in the murine model that resembles chronic human disease, innate immunity to mycoplasma requires IFN-γ when there are NK-like cells and the positive effects of IFN-γ counteract negative effects of NK-like cells. When imbalanced, NK-like cells promote disease. Thus, it was not the lack of IFN-γ but the presence of a previously unrecognized NK-like cell-suppressive activity that contributed to the higher mycoplasma numbers. It appears that pulmonary NK cells may contribute to the immunosuppressive environment of the lung, but when needed, these dampening effects can be counterbalanced by IFN-γ. Furthermore, there may be instances where perturbation of this regulatory balance contributes to the susceptibility to and severity of disease.
机译：这项研究的目的是检查与野生型BALB / c小鼠相比，γ干扰素敲除（IFN-γ？/？）小鼠的肺支原体水平差异100倍感染后3天。 NK细胞分泌IFN-γ;然而，它们的细胞毒性颗粒提取物未能杀死支原体。我们发现了一个难题：在清除NK的IFN-γ？/？动物中清除微生物与在野生型小鼠（同时使用IFN-γ和NK细胞）中一样有效。 NK + IFN-γ？/？动物支原体负担较高，但在NK样细胞耗竭后，支原体数量得到控制。基本上，IFN-γ在具有NK样细胞的动物中很重要，而在没有NK细胞的动物中则不重要，这表明IFN-γ可以抵消NK样细胞的有害作用。 IFN-γ？/？小鼠的先天免疫力降低不是由于巨噬细胞的NK样细胞杀伤。 NK细胞耗竭后，NK + IFN-γ？/？小鼠肺液中炎性细胞因子和中性粒细胞的升高水平降低。总之，在类似于慢性人类疾病的鼠模型中，当存在NK样细胞时，对支原体的先天免疫需要IFN-γ，而IFN-γ的阳性作用抵消了NK样细胞的阴性作用。当失衡时，NK样细胞会促进疾病。因此，并非是由于缺乏IFN-γ，而是由于存在先前无法识别的NK样细胞抑制活性，导致了较高的支原体数量。看来肺NK细胞可能有助于肺的免疫抑制环境，但是当需要时，这些抑制作用可以被IFN-γ抵消。此外，在某些情况下，这种调节平衡的紊乱会加剧疾病的易感性和严重性。

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